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Liver Cancer 3.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 April 2025 | Viewed by 1680

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Institute of Genetics and Animal Biotechnology of the Polish Academy of Sciences, 05-552 Jastrzebiec, Poland
Interests: transcription factors; epigenetics; gene mutation; cancer stem cell; molecular biology
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Special Issue Information

Dear Colleagues,

Liver cancer is one of the most common cancers and is the leading cause of death worldwide. Since there are no subjective symptoms in the early stages, it is generally at quite an advanced stage when it is discovered. Chronic liver damage often sets the stage for the oncogenic transformation of liver cells, giving rise to liver cancer. Risk factors for this transformation include excessive smoking, alcohol consumption, and hepatitis B and C viral infections, all of which can cause mutations in healthy DNA. These mutations can result in the deregulation of genes involved in controlling cell growth, cell death, and cell differentiation, thereby contributing to liver carcinogenesis. In this Special Issue, we will try to provide information which will be beneficial for non-specialist scientists to medical doctors in the field of liver cancer research. We will mainly consider, but are not limited to, the topics listed below.

Dr. Hiroaki Taniguchi
Guest Editor

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Keywords

  • liver cancer and mutations/genetics
  • liver cancer and gene regulation
  • liver cancer and stem cells
  • liver cancer and obesity
  • liver cancer and stress
  • liver cancer and clinical trials/therapies
  • liver cancer and epigenetic gene regulation
  • liver cancer and NASH
  • liver cancer and virus
  • liver cancer and immunology
  • liver cancer and 3D environment
  • liver cancer and microbiome

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Published Papers (1 paper)

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Research

18 pages, 4067 KiB  
Article
CRKL Enhances YAP Signaling through Binding and JNK/JUN Pathway Activation in Liver Cancer
by Marie C. Wesener, Sofia M. E. Weiler, Michaela Bissinger, Tobias F. Klessinger, Fabian Rose, Sabine Merker, Marcin Luzarowski, Thomas Ruppert, Barbara Helm, Ursula Klingmüller, Peter Schirmacher and Kai Breuhahn
Int. J. Mol. Sci. 2024, 25(15), 8549; https://doi.org/10.3390/ijms25158549 - 5 Aug 2024
Viewed by 1253
Abstract
The Hippo pathway transducers yes-associated protein (YAP) and WW-domain containing transcription regulator 1 (WWTR1/TAZ) are key regulators of liver tumorigenesis, promoting tumor formation and progression. Although the first inhibitors are in clinical trials, targeting the relevant upstream regulators of YAP/TAZ activity could prove [...] Read more.
The Hippo pathway transducers yes-associated protein (YAP) and WW-domain containing transcription regulator 1 (WWTR1/TAZ) are key regulators of liver tumorigenesis, promoting tumor formation and progression. Although the first inhibitors are in clinical trials, targeting the relevant upstream regulators of YAP/TAZ activity could prove equally beneficial. To identify regulators of YAP/TAZ activity in hepatocarcinoma (HCC) cells, we carried out a proximity labelling approach (BioID) coupled with mass spectrometry. We verified CRK-like proto-oncogene adaptor protein (CRKL) as a new YAP-exclusive interaction partner. CRKL is highly expressed in HCC patients, and its expression is associated with YAP activity as well as poor survival prognosis. In vitro experiments demonstrated CRKL-dependent cell survival and the loss of YAP binding induced through actin disruption. Moreover, we delineated the activation of the JNK/JUN pathway by CRKL, which promoted YAP transcription. Our data illustrate that CRKL not only promoted YAP activity through its binding but also through the induction of YAP transcription by JNK/JUN activation. This emphasizes the potential use of targeting the JNK/JUN pathway to suppress YAP expression in HCC patients. Full article
(This article belongs to the Special Issue Liver Cancer 3.0)
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